Up until 2006, the answer to this question by the vast majority of experts in obstetrics would have been a resounding “No!” In fact, the majority of the obstetrical literature still indicates that this is the case. However new work by several investigators (Gudmundsson 2005, Mazouni 2006) has confirmed a linkage between maternal size, fetal weight, and shoulder dystocia. Moreover, based on this principle, Dr. Emily Hamilton in Montréal appears to have developed a means by which the majority of those pregnant women destined to have a shoulder dystocia can be detected (Dyachenko, Hamilton 2006).

It must be emphasized that this predictive tool -- called the CALM Shoulder ScreenTM (patent pending) -- is currently undergoing its first clinical applications. It has not been available to obstetricians in the past, and is by no means the current standard of care. However, if the results thus far demonstrated by this predictive technique continue to be validated, the standard of care for the preventative management of shoulder dystocia may soon change.

First, however, let’s review the data that obstetricians have had up until now in attempting to predict which mothers and babies would experience shoulder dystocia.

In the past, there have been physicians who have claimed that shoulder dystocia could be predicted. Hassan (1988) stated,

"In the majority of cases shoulder
dystocia can be anticipated. Risk factors include maternal
obesity, diabetes, preeclampsia, prolonged gestation, and
fetal macrosomia. A male infant is at a greater risk for
macrosomia and dystocia."

However, this has been an overwhelmingly a minority opinion. The vast majority of obstetricians, including those who have done the most work on shoulder dystocia and brachial plexus injuries, up till now have concluded that it is impossible with any degree of certainty to predict in which deliveries shoulder dystocia will occur. The key issue involved is "certainty". As will be shown, there are multiple "risk" factors for shoulder dystocia. Mothers and babies having these risk factors are, in an absolute sense, more likely than mothers and babies without these factors to experience shoulder dystocia. But whether the predictive value of such factors as currently measured is high enough to be useful clinically, that is, to justify changes in labor management plans in hopes of avoiding shoulder dystocia, is what is at issue. Moreover, as with most statistical questions in medicine, the predictability of shoulder dystocia has to be looked at from two directions:

Sensitivity: Are the risk
factors associated with shoulder dystocia able to accurately
identify most babies who will have shoulder dystocia at
birth?

Positive predictive value:
What percentage of mothers and babies having these risk
factors will, in fact, experience shoulder dystocia?

In the case of shoulder dystocia, its infrequent rate of occurrence (0.5%) and the low positive predictive value of risk factors for it have severely impeded the ability of obstetricians to utilize such information to advantageously alter clinical care.

The past medical literature has confirmed this overwhelmingly. Gherman (2002), among current leaders in the study of shoulder dystocia, has said the following:

Most of these preconceptions and
prenatal risk factors have extremely poor positive
predictive values and therefore do not allow the
obstetrician to accurately and reliably predict the
occurrence of shoulder dystocia.

Resnick (1988), discussing the ability of obstetricians to predict when shoulder dystocias will occur, stated that "the diagnosis [of shoulder dystocia] will often be made only after delivery of the fetal head."

Lewis (1998) noted that only 25% of shoulder dystocia cases had at least one significant risk factor.

Geary (1995) reported that when all antenatal risk factors for shoulder dystocia were taken into account, the positive predictive value was less than 2% for individual factors and less than 3% when multiple factors were combined.

The bottom line is this: In the past, nowhere in the literature were there studies that showed that the sensitivity or positive predictive value for predicting shoulder dystocia was high enough to justify obstetrical interventions in hopes of avoiding it.

Categories of risk factors

The risk factors for shoulder dystocia
can generally be divided into three categories:

Preconceptual -- before
pregnancy

Antepartum -- during
pregnancy

Intrapartum -- during labor
and delivery

Preconceptual risk factors for
shoulder dystocia

1. Previous shoulder dystocia

Previous shoulder dystocia proves to
be one of the most accurate predictors for recurrent shoulder
dystocia. This makes perfect sense. The pelvic anatomy of a
woman does not change in between pregnancies. Moreover, second
and subsequent babies are likely to be larger than first or
previous babies.

The risk of a woman having a repeat
shoulder dystocia once having had one, as reported from
various authors, is:

Smith (1994) 12%

Ginsburg (2001) 11%.

Gherman (2002) 11.9%

This compares with the baseline risk
for shoulder dystocia of 0.5%. Because of this significant
increase in risk -- approximately 20-fold -- some obstetricians
have proposed "once a shoulder dystocia, always a cesarean".

2. Maternal obesity

A mother's weight, likewise, proves to
be significantly correlated with shoulder dystocia. Emerson
showed (1962) that in his series shoulder dystocia occurred
twice as often in obese women as it did in normal weight
women: 1.78% versus 0.81%. Sandmire (1988) estimated that the
relative risk of shoulder dystocia in women with a
prepregnancy weight of greater than 82 kg (181 lbs) was 2.3.

However whether this is a primary
effect or merely reflects the fact that obese women tend to
have large babies is not clear. To answer this question would
require a study evaluating the rates of shoulder dystocia
correlated with both maternal and fetal weight categories.
Given the fact that more pregnant women than ever are obese,
and that obesity has a marked correlation with fetal
macrosomia, it is likely that the rate of shoulder dystocia
will be seen to increase over the next decade.

But there are major problems with attempting to use obesity by itself as a predictor of shoulder dystocia. Although obese women do have an incidence of shoulder dystocia several fold higher than that of thinner women, even the most pessimistic reports -- such as that by Hernandez in 1990 -- show a rate of shoulder dystocia in women weighing over 250 lbs. of no more than 5%. Thus even in this high risk population, 95% of extremely obese women will not have a shoulder dystocia at delivery. Thus any intervention undertaken based solely on the relationship between maternal weight and macrosomia would be without justification for 19 of 20 of such women.

3. Maternal age

Some studies have claimed maternal age
to be a risk factor for shoulder dystocia. But careful
analysis reveals that maternal age is a risk factor for
shoulder dystocia only in so far as maternal obesity,
diabetes, excessive weight gain, and instrumental deliveries
are all more common in older women. These, of course, are all
themselves risk factors for shoulder dystocia. In one of the
few studies looking at the correlation between maternal weight
and shoulder dystocia in isolation, Bahar (1996) did not find
any difference in shoulder dystocia based on maternal age
alone.

4. Abnormal pelvis

O'Leary, in his book on shoulder
dystocia, places great significance on the abnormal pelvis as
a risk factor for shoulder dystocia -- but offers no data to
support his claim. Although it would make sense that a
decrease in certain pelvic dimensions would increase the
possibility of a baby's anterior shoulder getting caught on
the maternal pubic bone, there are no reports in the
literature demonstrating a relationship between shoulder dystocia and objectively-measured pelvic shape.

Moreover, the use of pelvimetry -- x-ray
or other measurement of pelvic dimensions -- in obstetrics was
discarded years ago, for several reasons:

1. Except in the very most extreme
cases of congenital or pathological pelvic deformity, there is
poor correlation between pelvic size and a woman's capacity to
delivery vaginally.

2. The ability to more accurately
monitor babies in labor enables obstetricians to safely allow
labor itself to be the test of whether or not a baby will
"fit" into and through the maternal pelvis.

5. Multiparity

In a 10-year series collected from
Boston's Beth Israel Hospital covering the years 1975 to 1985,
Acker (1988) showed that there were more Erb palsies in babies
born to multiparous women then to primigravida women. He
attributed this to a marked increase in precipitous labors in
such women. In his series he noted that 31.8% of all babies
with Erb palsy had experienced a precipitous delivery.

But as with maternal age, by the time
a woman becomes "multiparous", she is old enough to have an
increased risk of having other risk factors for shoulder
dystocia such as larger babies, obesity, and diabetes.
Moreover, only multiparous women could have the very
significant risk factor of having had a previous shoulder
dystocia. Thus most experts feel any relationship between
multiparity and shoulder dystocia is secondary to other, more
primary, risk factors.

Shoulder dystocia is seen more
commonly with increased maternal age, obesity, and multiparity
-- but
in reality these are only markers for the increased risk of
more primary risk factors

There is no evidence linking the
"abnormal pelvis" to shoulder dystocia

B. Antepartum factors risk factors for
shoulder dystocia

1. Macrosomia

Macrosomia is far and away the most
significant risk factor for shoulder dystocia. It is the
factor that has been most studied and most often proposed as a
potential target for manipulation in hopes of reducing the
number of shoulder dystocia deliveries. Some authors go so far
as to claim that no other risk factor has any independent
predictive value for the occurrence of shoulder dystocia.

The most obvious confirmation of this
relationship consists of those studies measuring the
percentage of babies in different weight groups that
experienced shoulder dystocia. What is vitally important to
keep in mind when considering such data, however, is that
these are the weights ascertained after delivery. They were
not available to the obstetrician before delivery in making
his or her clinical decisions as to how the delivery should be
conducted.

Acker (1985) found that babies
weighing over 4500gms experienced shoulder dystocia 22.6% of
the time. The shoulder dystocia rate in his general population
was 2%. His report showed the following:

Infant
weight in Nondiabetic women

Percent shoulder dystocia

Less than 4000 g

1.1%

4000g - 4499 g

10.0%

Greater than 4500 g

22.6%

More than 70% of all shoulder
dystocias in his study occurred in infants weighing more than
4000 g.

Kolderup (1997), in a review of 2924
macrosomic deliveries at UCSF, reported that macrosomic
infants have a six fold increase in significant injury from
shoulder dystocia deliveries compared with controls.

Jackson (1988) showed in his series of
8258 deliveries that the average birth weight of babies who
suffered brachial plexus injuries was 4029 g., whereas the
average birth weight of all deliveries was 3160 g,

Lazer (1986) reported that the
shoulder dystocia rate for infants weighing more than 4500 g
was 18.5% while for "smaller babies" in his series the rate
was 0.2%.

The definition of macrosomia has
varied both through the years and according to the author
writing about it. The various cutoff points used to define
macrosomia have been 4000 g, 4500 g, and 5000 g. Often a
distinction has been made between macrosomia in nondiabetic
versus diabetic mothers, the bar being set lower for the
fetuses of diabetic mothers. In general, in babies born to
nondiabetic mothers 5% to 7% will weigh more than 4000 g; 1%
will exceed 4500 g.

One of the most important factors
about macrosomia is the differential rate of growth of the
fetal head, chest, and trunk as gestation proceeds, both in
the babies of diabetic and of nondiabetic mothers. Until 36-38
weeks, the fetal head generally remains larger than the trunk.
Between 36 and 40 weeks, however, the relative growth of the
abdomen, chest, and shoulders begins to exceed that of the
fetal head. This is especially the case in babies of diabetic
mothers where glucose substrate levels are higher in both the
mother and fetus. Thus both in prolonged gestation and in
babies of diabetic mothers the size of a baby's trunk is
likely to increase, increasing its chances of shoulder
dystocia.

How is fetal weight predicted and
how accurate are these predictions?

Although the correlation between fetal
weight and shoulder dystocia is of great interest to
obstetricians, knowing about this relationship is of no use
unless fetal weight -- and the corresponding increased risk of
shoulder dystocia -- can be predicted prior to delivery. How
good, therefore, are our current techniques for estimating
fetal weight?

Traditionally, fetal weight has been
estimated by measurement of uterine height and by Leopold
maneuvers. "Leopold maneuvers" is the name given to palpation
of the maternal abdominal wall a series of four specific steps
in order to determine fetal position, fetal presentation, and
an estimate of the size of the baby.

Such estimates, however, are
notoriously inaccurate. Studies have shown grave discrepancies
between estimation of fetal weight by experienced
obstetricians and actual fetal weight at delivery. Moreover
these studies show that the same obstetrician will make
different estimates of fetal weight on the same maternal
abdomen when repeatedly checked at close intervals.

With the advent of ultrasonic fetal
evaluation in the 1970's, it was hoped that a more accurate
means of assessing fetal weight was at hand. Many papers were
published presenting various formulas for ultrasound
estimation of fetal size. Most of these involved some
combination of measurements of fetal head and abdominal
dimensions and fetal femur length. However comprehensive
analyses of these various ultrasound formulas have concluded
that none are consistently more accurate than being within 10
to 15% of actual birth weights. Chauhan in 1995 went so far as
to say that in more than half of the models for ultrasound
prediction, clinical predictions by obstetricians were as or
more accurate. This was found to be especially true in larger
babies:

From these data it appears that
sonographic models are not significantly superior to clinical
examination in detecting newborns with birth weight's greater
than or equal to 4000 g.

Another study by Chauhan (1992) showed
that pregnant women themselves were more accurate than either
ultrasound or physician clinical estimates in determining the
birth weights of their infants.

There are many studies that confirm
the inability of any current diagnostic technique to determine
fetal weight prior to birth to any better than 10-15% above or
below the true weight:

Delpapa (1991): Only 48% of estimates
of fetal weight as determined by ultrasound within three days
of birth were within 500 g of the final fetal weight.

Benson (1987): The use of ultrasound
formulas to predict macrosomia was correct in only 47% of
infants.

Jazayeri (1999): Using a formula based
on ultrasound abdominal circumference in an attempt to
determine which babies would weigh over 4500gmshe obtained a
positive predictive value of only 9%.

Shoulder/chest/abdomen ratios

As discussed above, post term growth
and maternal diabetes result in the fetal trunk growing larger
relative to the fetal head. The same pattern of
disproportionate growth occurs with babies that are large for
any reason, including inherent genetic predisposition. This is
why macrosomic babies have a higher incidence of shoulder
dystocia. In a normally proportioned baby, once the head is
delivered the fetal shoulders and body usually deliver easily.
With shoulders and trunk bigger than the fetal head, it is
much more likely that they will get stuck.

Several investigators have sought to
measure the differences in size between fetal shoulders,
trunks, and head circumferences to see if there existed a
certain ratio at which the risk of shoulder dystocia became
prohibitively high. Hopewood (1982) proposed that when the
transthoracic diameter is 1.5 cm larger than the biparietal
diameter, shoulder dystocia would be significantly increased.
Kitzmiller in 1987 developed a formula involving a CT scan of
fetal shoulders by which he was able to predict fetal weight
with good accuracy: a positive predictive value of 78% for
predicting birth weights over 4200 g. with a negative
predictive value of 100%.

However, several authors have refuted
the utility of using the relationship between measurements of
different anatomic structures to predict shoulder dystocia.
Benson (1986), while acknowledging that femur length/abdominal
circumference ratios differ in macrosomic vs. nonmacrosomic
fetuses, claimed that there is too much overlap between the
larger and smaller groups in any formula protocol to be
clinically useful. He states in his paper that "for no cutoff
value of these measurements is there a high sensitivity and
high specificity."

Thus the question: Can shoulder
dystocia be reliably predicted by estimating fetal weight?

The problems with attempting to
estimate which fetuses will be macrosomic and using this
information as a tool for predicting shoulder dystocia are
twofold:

In the first place, it is the general
conclusion of most obstetrical experts who have studied this
issue that predicting macrosomia is unreliable. If macrosomia
cannot be reliably determined, it is hard to try to use it to
predict shoulder dystocia.

Secondly, only a very small percentage
of babies, even of those who have macrosomia, go on to develop
shoulder dystocia. This presents a significant obstacle to the
use of estimates of fetal weight as a tool for deciding when
to change clinical management in hopes of preventing shoulder
dystocia deliveries.

These difficulties are highlighted in
the data presented below:

Resnick (1980) found that shoulder
dystocia occurred in only 1.7% of 1409 infants born at Johns
Hopkins Hospital weighing more than 4000 g.

Acker (1986) pointed out that although
the relative frequency of shoulder dystocia varied directly
with increasing birth weight, almost half of the shoulder
dystocias occurred in deliveries involving average and smaller
babies. This is because there were so many more of them.
Forty-seven percent of all shoulder dystocias at the Beth
Israel hospital during the time of his study occurred in
babies weighing less than 4000 g, a weight category which
encompassed 91.2% of his total delivery population. Thus any attempt to use estimates of fetal weight as an isolated factor to reduce the incidence of shoulder dystocia would miss half of all shoulder dystocias -- even if macrosomia could be accurately measured.

Gonen (2000) evaluated 17 babies with
brachial plexus injuries from a population of 16,416
deliveries. Only three of these injured babies were macrosomic.

Geary (1995) found that the positive
predictive value of a birth weight of more than 4000 g for
predicting shoulder dystocia was only 3.3%.

Delpapa's 1991 study showed that, at
his institution, 50% of babies estimated to weigh more than
4000gm in fact had birth weights below 4000gm -- a false positive
rate for predicting macrosomia of 50%!

Levine in 1992 showed that if
macrosomia was defined as the 90th percentile of fetal weight
for a given gestational age, then sonographic prediction of
macrosomic was wrong 50% of the time both in underestimating
and overestimating fetal weight. Similar unsuccessful attempts
to accurately ascertain fetal birth weight during the
antenatal or intrapartum period have been published by:

Sandmire (1993)

Sacks DA (2000)

Boyd (1983)

Chauhan (1992)

Levine (1992)

The American College of Obstetricians
and Gynecologists bulletin on shoulder dystocia states that
ultrasound has a sensitivity of only 22 to 44% and a positive
predictive value of only 30 to 44% in predicting macrosomia.

Thus up until now, as has been shown, it has been the general consensus of obstetricians who have done research in the area of shoulder dystocia that the occurrence of shoulder dystocia based on estimations of fetal weight could not be reliably predicted.

El Madany sums up this issue well in
his 1990 paper:

"Even if certain combinations of risk
factors exist which could with high likelihood isolate which
babies experienced shoulder dystocia, the inability to predict
macrosomia with the requisite degree of certainty on which
such a clinical suspicion is based precludes making active
action protocols. Until the macrosomic infant can be
accurately identified, no reasonable risk factor profile can
be established."

Sandmire, in his 1993 article,
concludes:

"Any approach using ultrasound would
have to demonstrate that its use improves newborn or maternal
outcome without disproportionate increases in morbidity and
mortality. A barrier to achieving this goal is the inaccuracy
associated with ultrasonic estimations of fetal weight. The
current ultrasonic procedures for estimation of fetal weight
are not accurate enough for detecting macrosomia defined by
weight criteria. And even if clinicians could determine fetal
weight accurately, the frequency of persistent fetal injuries
associated with vaginal birth of the macrosomic fetus is so
low that induction of labor or cesarean birth is not justified
on that basis. Delivery decisions based on inaccurate
estimated fetal weight should be avoided."

Thus, while macrosomia is a major risk factor for shoulder dystocia, it has not been possible to accurately predict shoulder dystocia by attempting prediction of macrosomia.

click on
image to view larger image

2. Diabetes

Next to macrosomia, the factor most
closely associated with shoulder dystocia is maternal diabetes
in pregnancy. One of the first clear-cut demonstrations of
this was Acker's 1985 paper showing the following:

Estimated fetal wt.

Nondiabetic mothers
% shoulder dystocia

Diabetic mothers
% shoulder dystocia

< 4000 g

1.1%

3.7%

4000-4499 g

10.0%

30.6%

> 4500 g

22.6%

50%

As can be seen, babies of diabetic
mothers had a three to fourfold increase in the risk of
shoulder dystocia compared to babies of nondiabetic mothers in
each weight category.

Although diabetic mothers accounted
for only 1.4% of the birth population in this study, they
accounted for 4.9% of shoulder dystocias. Acker also showed
that although the general rate of Erb palsy following shoulder
dystocia is roughly 10%, 17% of babies born to diabetic
mothers developed Erb palsy.

Other investigators have shown similar
or larger correlations between diabetes and shoulder dystocia.
In Al-Najashi's study (1989), the rate of shoulder dystocia in
babies weighing over 4000gm born of diabetic mothers was
15.7%. Babies born to nondiabetic mothers had a shoulder
dystocia rate of 1.6%.

Casey (1997), in a study of over
62,000 patients, found the shoulder dystocia rate in his
general obstetrical population to be 0.9% while in his
patients with gestational diabetes it was 3%.

Sandmire (1988) found a relative risk
for shoulder dystocia in the babies of diabetic mothers of 6.5
compared to nondiabetic mothers.

There are two main reasons for this
correlation between diabetes and shoulder dystocia. In the
first place, diabetes in pregnancy shows a very strong
correlation with macrosomia. The growth of diabetic babies
represents not only their genetic potential for growth but
also reflects the laying down of extra glucose substrates
present in both the mother and baby. Secondly, as previously
mentioned, the nature of the fetal growth differs in diabetic
babies. Growth is not as evenly distributed between the head
and trunk as it is in nondiabetic babies. Rather, babies of
diabetic mothers show a pattern of greater shoulder, chest,
and abdominal growth. As Ellis summarized in 1982:

"The infant of a diabetic mother has a
different body configuration than the infant of a nondiabetic
mother. Increased deposition of fat in various organs may be
due to increased insulin secretion in response to
hyperglycemia."

Can shoulder dystocia be predicted in
babies of diabetic mothers?

In the 1980s several authors published
studies purporting to show that they could predict which
babies of diabetic mothers would be at high risk for shoulder
dystocia.

Elliott (1982) claimed that by
evaluating the chest-biparietal diameter in infants of
diabetic mothers weighing more than 4000 g, he could reduce
the incidence of traumatic morbidity at delivery from 27% to
9%.

Tamura (1986) found that in diabetic
women fetal abdominal circumference values greater than the 90
percentile correctly predicted macrosomia in 78% of cases. In
his study, when both the abdominal circumference and the
estimated fetal weight exceeded the 90th percentile in
pregnant women with diabetes, macrosomia was correctly
diagnosed 88.8% of the time.

Mintz, in a promising study from 1989,
published data showing that in his hands a combination of
fetal abdominal circumference > the 90th percentile for
gestational age and shoulder soft tissue width greater than 12
mm was the best predictor of macrosomia. His data reported a
sensitivity of 96%, specificity of 89%, and
"accuracy" -- positive predictive value -- of 93%. He also found a
significant correlation between shoulder width and a high
HgA1C, a blood test that measures blood sugar control over the
preceding three months.

Unfortunately, these results have not
been supported or replicated by other investigators. Multiple
experts in the field of shoulder dystocia have published data
from very large series that absolutely contradict the
conclusions listed above. In addition, the results of these
studies are not as powerful as might first be assumed.

In Elliott's study, for instance,
although he was able to show that a large number of babies
meeting certain chest-biparietal diameter criteria were
macrosomic, 39% of babies with these same parameters -- chest/biparietal
diameter ratio of > 1.4 -- were not larger than 4000 g. In
Tamura's steady, although he was able to predict macrosomia in
babies meeting certain abdominal circumference criteria, he
still was unable to identify the vast bulk of macrosomic
fetuses. As for Mintz's study, no one has yet been able to
duplicate his results.

In fact, most past studies have found that neither macrosomia nor shoulder dystocia can be reliably predicted in the babies of diabetic mothers. Acker (1985) showed that by using the criteria of large baby and diabetic mother he could predict 54.7% of shoulder dystocias -- but would miss 45.3% of them (false negatives). Delpapa (1991) stated that the predictive value of estimated fetal weight in babies of diabetic mothers for predicting shoulder dystocia was not sufficient to reliably identify them.

Moreover, most diabetic mothers do not
have macrosomic babies and the overwhelming majority of
macrosomic infants are not babies of diabetic mothers. The
bottom line is that macrosomia is as difficult to predict in
diabetic mothers as it is in the nondiabetic population.

There are two other studies of
interest relating to this question.

Coen (1980) showed that although
HgbA1C is a good marker for long-term monitoring of blood
sugars in diabetic patients, it is not a good predictor of
large-for-gestational age infants. The average HgA1C in
mothers of large-for-gestational age infants in his study was
6.7; for mothers delivering normal sized babies the average
HgA1C was 6.5 -- too close to be clinically useful.

Casey (1997) reported that although
the rate of shoulder dystocia was in fact increased in mothers
with gestational diabetes, this was not manifest in an
increase in the rate of Erb palsy.

The bottom line: Predicting macrosomia and shoulder dystocia in diabetic mothers has been as difficult as predicting these factors in the nondiabetic population.

Abrams (1995) and Langhoff-Roos (1987)
both showed that total maternal weight gain was significantly
correlated with infant birth weight. Dawes (1991), however,
was not able to confirm this:

There was no apparent difference in
correlation between maternal weight gain and birth weight
between women giving birth to average for gestation or large
for gestational age infants

Moreover, several investigators have
reported conflicting information as to the effect of patterns
of maternal weight gain on ultimate fetal weight. Some studies
have found second trimester weight gain to be the major
determinate whereas others have found that the weight gain in
the last trimester was the most important factor. Given the
contradictory and confusing data on this subject, Dawes'
(1991) closing statement is probably the most apt:

"The variations in total (maternal)
weight gain and incremental weight gain are so wide that these
measurements are unlikely to be clinically useful."

4.. Fetal sex

There is little data correlating fetal
sex with macrosomia and shoulder dystocia. Although on average
male babies do weigh slightly more than females, there is no
data showing a significantly higher number of macrosomic male
infants than female infants.

Resnick in his classic 1980 paper
mentions fetal sex as a potential factor but does not supply
data to substantiate his claim. El Madany (1990) showed that
59.2% of babies experiencing shoulder dystocia in his study
were male -- statistically significant but not of much value as a
clinical predictor.

5. Multiparity

Any relationship thus far observed
between multiparity and either macrosomia or shoulder dystocia
has been linked to the fact that multiparous women are, on
average, older and heavier than primigravida women. They are
therefore more likely to have larger babies and are more
likely to have or develop diabetes, both of which would
increase the risk of shoulder dystocia. In addition, by
definition multiparous women have already had one or more
babies. Thus they may already have experienced a shoulder
dystocia which of course would place them at greater risk for
recurrent shoulder dystocia.

The only primary association between
multiparity and shoulder dystocia is the fact that multiparous
women are more likely than primiparous women to have
precipitous labors. This has been linked by several
investigators (Gonen [2000], Acker [1988]) to an increased
risk of shoulder dystocia.

6. Post-dates

Even though fetal growth slows in the
last several weeks of pregnancy, there is still some growth as
long as pregnancy continues. Thus the longer the baby remains
in utero, the larger the baby will be -- and the greater the risk
of shoulder dystocia. Acker (1985) was one of the first to
demonstrate this association. Chervenak confirmed this in 1989
when he reported that 25.5% of babies delivering at 41 weeks
gestation were macrosomic while only 6% (risk ratio 4.2) were
macrosomic in a group delivering between 38 and 40 weeks
gestation. Hernandez (1990), too, found a direct correlation
between post date babies and an increased risk of shoulder
dystocia. He attributed this entirely to the increased
tendency of post-date babies to be macrosomic.

Multiple risk factors

The greatest risk for shoulder
dystocia occurs in those groups of women who have multiple
risk factors. An obese woman with a large pregnancy weight
gain and gestational diabetes will have a significantly
greater likelihood of having a macrosomic baby and shoulder
dystocia than will a woman who has just one of these risk
factors. The worst possible combination of risk factors would
be a mother with diabetes, an estimated large-for-gestational-age fetus, a prolonged second stage of labor,
and a forceps delivery (to be discussed below). The rate of
shoulder dystocia in such a situation approaches 40%.

Summary of antepartum risk factors

Macrosomia and maternal diabetes are
the main risk factors for shoulder dystocia

Predicting fetal weight is
extremely unreliable

Other factors -- maternal weight gain,
fetal sex, and post dates -- are secondary risk factors. They do
indicate an increased risk for shoulder dystocia but they are
only relevant to the degree that they increase risk of fetal
macrosomia

Since multiparity increases the
number of precipitous labors it may be a primary risk factor
for shoulder dystocia

Intrapartum risk factors

Various characteristics of labor and
delivery have been claimed to be useful in predicting whether
or not a given mother-baby pair will end up with a shoulder
dystocia and possible brachial plexus injury.

1. Instrumental delivery

Several studies have clearly shown
that labors that end in instrumental vaginal
deliveries -- vacuum or forceps -- show a higher rate of shoulder dystocia in each fetal weight group.

Benedetti reported that in deliveries
with the combination of a prolonged second stage of labor and
a mid pelvic delivery there was a 4.6% rate of shoulder
dystocia -- compared to 0.4% when there was neither prolonged
second stage nor mid pelvic delivery.

McFarland (1986) showed that the
relative risk of brachial plexus injury was 18.3 for
midforceps deliveries and 17.2 for vacuum deliveries when
compared to unassisted vaginal deliveries.

Thus it is clear that deliveries
requiring instrumental assistance have a higher risk of
shoulder dystocia and brachial plexus injury. It is not clear,
however, that it is the instrumental deliveries themselves
that are to blame for these shoulder dystocias. It may well be
that the mother's inability to push the baby out without
assistance is due to fetal macrosomia or an altered
distribution of fat between the fetal head, chest, shoulders,
and abdomen -- themselves major risk factors for shoulder dystocia.

2. Experience of the deliverer

Since the safe resolution of a
shoulder dystocia involves specific obstetrical maneuvers and
since shoulder dystocias occur relatively infrequently, it
would seem that more experienced practitioners would have
better outcomes in these situations merely by virtue of having
seen more of them. Such an opinion would surely be voiced by
most obstetricians and experienced labor and delivery nurses.
However the data does not support this belief.

In the only study that has looked at
the experience of the deliverer in relation to shoulder
dystocia, that by Acker in 1988, the number of Erb palsies
following shoulder dystocia deliveries did not vary with
either the number of years a physician had been in practice or
the number of deliveries that physician performed. As Acker
stated,

Most clinicians hardly gain expertise
and confidence in the difficult

manipulations required to resolve
shoulder dystocia due to the rarity of the condition.

3. Labor abnormalities

Several studies have shown a higher
incidence of shoulder dystocia in labors in which the second
stage of labor is prolonged. Nevertheless -- and
paradoxically -- shoulder dystocias are not infrequently seen
during labors with very rapid second stages.

Al-Natasha (1989) found that a delay
in the second stage of labor and slowed descent of the fetal
head in an obese multiparous woman greatly increased the
possibility that a shoulder dystocia would occur.

Hopewood (1982) found that there was a
deceleration phase of active labor from eight to 10 cm in 58%
of shoulder dystocia deliveries.

No particular labor abnormality was
predictive of an increased incidence of shoulder dystocia
relative to that encountered with a normal labor pattern, a
spontaneous delivery, or both.

Lurie (1995) also found no correlation
between length of the stages of labor and shoulder dystocia.
He showed that there was no difference in (1) the mean rate of
dilatation, (2) the percentage of protracted labors, or (3)
the mean duration of the second stage of labor in a group of
mothers who experienced shoulder dystocia deliveries versus a
group that delivered without complication. His conclusion was
that protracted labor did not seem to be a risk factor for
shoulder dystocia. As he says in his paper,

One could not identify shoulder
dystocia in advance while analyzing the rate of cervical
dilation or duration of the second stage of labor.

Hernandez (1990) reported that
although there is a relationship between the length of various
stages of labor and shoulder dystocia, 70% of patients who
experienced shoulder dystocia had normal labor patterns.

McFarland (1975) likewise reported the
same rate of labor abnormalities of the active phase of labor
and of the second stage of labor in both shoulder dystocia and
control groups. He concluded that labor abnormalities could
not serve as clinical predictors for the subsequent
development of shoulder dystocia.

Even if disorders of labor were found
to be correlated with shoulder dystocia, it is not clear
whether this would represent an independent risk factor. It
might merely confirm that labor disorders are more common with
macrosomic babies and that macrosomic babies more commonly
experience shoulder dystocia. To date there has been no major
study evaluating the length of various stages of labor broken
down by weight category in relationship to shoulder dystocia
deliveries.

To further complicate the issue, it is
well known that shoulder dystocias and brachial plexus
injuries are often seen with short second stages of labor:

Gonen (2000) reported that 7 of 17
patients (41%) with brachial plexus injury had second stages
of labor shorter than 10 minutes

Acker (1988) found that 31.8% of all
babies with Erb palsy were born after precipitate second
stages of labor. As he explains,

The rapidity of descent may prohibit
the fetal shoulders from entering the inlet in an oblique diameter,
preclude adequate preparation for delivery, and add to nerve root trauma.

This phenomenon of shoulder dystocias
with rapid second stages of labor will be discussed in further
detail below.

4. Oxytocin and anesthesia

There does not appear to be any
independent correlation between the use of either oxytocin or
anesthesia and shoulder dystocia deliveries.

Oxytocin is generally used to increase
the strength of uterine contractions. To the extent that
oxytocin is used more frequently with macrosomic infants, it
might have a secondary correlation with shoulder dystocia
deliveries. But there is no published data linking oxytocin
use with the incidence of shoulder dystocia independent of
fetal weight.

Likewise with anesthesia, there is no
reported increase in shoulder dystocia deliveries in labors in
which conduction anesthesia is employed.

5. Episiotomy

There is no statistically significant
relationship between the absence of episiotomy, the frequency
of shoulder dystocia, and any subsequent neonatal injury. That
this is the case is perplexing given that almost all protocols
for the resolution of shoulder dystocia advocate making a
"generous episiotomy". This recommendation appears to be
without support in the literature.

There are two possible reasons one
might make an episiotomy in the case of a shoulder dystocia.

The first would be to make more room
for the baby to emerge. In this situation the indications for
making an episiotomy would be the same as in any delivery:
alleviating soft tissue dystocia of the perineum. If the
perineal tissue were tight, then an episiotomy might be
helpful in delivering the baby. However, if the soft tissue is
pliable and stretches easily, as in most multiparous women,
then an episiotomy will not make it any easier to free the
anterior shoulder from behind the pubic bone.

The second possible indication for an
episiotomy during a shoulder dystocia would be to allow more
room for the obstetrician's hand to move inside the pelvis in
performing the Wood screw maneuver or in attempting to deliver
the baby's posterior arm. An episiotomy might be helpful in
accomplishing these maneuvers in a woman whose perineal
tissues impede access to the fetal shoulders. However, in a
woman in whom the perineal tissues are lax enough to allow
these maneuvers to be performed, the automatic making of an
episiotomy will not facilitate delivery and would be
unnecessary.

Thus the almost universal
recommendation that an episiotomy be made during a shoulder
dystocia delivery is not only without literature support, but
is theoretically unsupportable as well.

So, can shoulder dystocia be reliably
predicted?

Up until this year, both the short and the long answer to this question would have been: "No". Nowhere in the literature were there studies that showed that the sensitivity or positive predictive value for predicting shoulder dystocia was high enough to justify interventions. While macrosomia, diabetes, prolonged second stage of labor, instrumental delivery, and other factors do indicate a statistically increased risk of having a shoulder dystocia, their low positive predictive value and high false positive rate make them clinically useless as tools for predicting -- and hence trying to prevent -- shoulder dystocia.

Below are the thoughts of various shoulder dystocia investigators on the predictability of this entity based on evidence that had been available up until this year (2006):

Basket (1995):
The profile of risk for shoulder
dystocia -- prolonged pregnancy, prolonged second stage of labor, macrosomia, and
assisted mid pelvic delivery -- were not clinically useful because the
large majority of cases of shoulder dystocia occur in patients without
these risk factors.

Resnick (1980):
Most babies with shoulder dystocia do
not have risk factors.

German (2002):
Most of these preconception and
prenatal risk factors have extremely poor positive predictive
values and therefore do not allow the obstetrician to
accurately and reliably predict the occurrence of shoulder dystocia.

As mentioned above, there is new research that has linked maternal size and fetal weight to the risk of shoulder dystocia. In addition, Dr. Emily Hamilton and her team of researchers in Montreal have developed a tool, based on sophisticated statistical and mathematical analysis of large numbers of shoulder dystocia cases, that can identify the majority of those mothers and fetuses destined to experience a shoulder dystocia.

The factors involved in this analysis of risk are maternal height, maternal weight, parity, gestational age, baby’s estimated weight, and maternal history of gestational diabetes or previous shoulder dystocia. Dr. Hamilton’s formula has been tested against several large independent samples of patients who had experienced shoulder dystocia with permanent injury. The data—some already published, some in the process of submission—shows that it is possible to consistently identify 50-70% of patients destined to have a shoulder dystocia with a false positive rate (rate of additional cesarean sections) of only 2.7%. (Dyachenko, Hamilton 2006)